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Expression data of GMP and MDP from wild-type and Trib1-/- mice

ABSTRACT: Trib1 is critical for some myeloid cell differentiation. Therefore we used microarrays to investigate gene expression profiles in wild-type and Trib1-/- progenitor of myeloid cells. Progenitor cells, such as GMP and MDP, obtained from wild-type and Trib1-/- mice were sorted, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

ORGANISM(S): Mus musculus

SUBMITTER: Takashi Satoh

PROVIDER: E-GEOD-43563 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data of GMP and MDP from wild-type and Trib1-/- mice

Project description:Trib1 is critical for some myeloid cell differentiation. Therefore we used microarrays to investigate gene expression profiles in wild-type and Trib1-/- progenitor of myeloid cells.

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Murine GMP- and MDP-derived classical monocytes have distinct functions and fates [dataset 1]

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The chromatin structures of GMP-MoPs are shifted toward ones that favors an aberrant differentiation pathway generating GMP-MoPs from proNeu1 [ATAC-seq]

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Trib1 promotes acute myeloid leukemia progression by modulating transcriptional programs of Hoxa9 [array]

Project description:The pseudokinase Trib1 functions as a myeloid oncogene that recruits E3 ubiquitin ligase COP1 to C/EBPa, and interacts with MEK1 to enhance ERK phosphorylation. Close genetic interaction between Trib1 and Hoxa9 has been observed in myeloid leukemogenesis as Trib1 overexpression significantly accelerates Hoxa9-induced leukemia onset. Yet the mechanism how Trib1 functionally modulates Hoxa9 transcription activity is unclear. Here we provide evidence that Trib1 modulates Hoxa9-associated super-enhancers. ChIP-seq analyses identified increased Histone H3K27Ac signals at the super-enhancers such as Erg, Aff3, Spns2 and Coro2 loci, as well as increased mRNA expression of these genes. The modification of super-enhancer activities is mostly achieved by degradation of C/EBPa by Trib1 and the MEK/ERK pathway only slightly contributes to the activities. Silencing of Erg abrogates the growth advantage acquired by Trib1 overexpression, indicating that Erg is a critical downstream target of the Trib1/Hoxa9 axis. Moreover, treatment of AML cells with the BRD4 inhibitor JQ1 showed growth inhibition in the Trib1/Erg-dependent manner. Upregulation of ERG by TRIB1 was also observed in human AML cell lines, suggesting that Trib1 is a potential target of Hoxa9-associated AML. We used microarrays to detail the global program of gene expression in mouse AML

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2020-10-21 | GSE140313 | GEO

TRIB1 suppression on human hepatocytes transcriptome

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2015-04-13 | E-GEOD-61473 | biostudies-arrayexpress

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